HIV-induced immunodeficiency. Relatively preserved phytohemagglutinin as opposed to decreased pokeweed mitogen responses may be due to possibly preserved responses via CD2/phytohemagglutinin pathway.
HIV-induced immunodeficiency. Relatively preserved phytohemagglutinin as opposed to decreased pokeweed mitogen responses may be due to possibly preserved responses via CD2/phytohemagglutinin pathway.
复制标题
HIV引起的免疫缺陷。
作者：
B. Hofmann;K. D. Jakobsen;N. Ødum;E. Dickmeiss;P. Platz;L. Ryder;C. Pedersen;L. Mathiesen;I. Bygbjerg;Viggo Faber
我们研究了301例HIV血清阳性的男同性恋者(其中55例患有艾滋病)的PBL对有丝分裂原PHA、PWM和白色念珠菌抗原的增殖反应。对PHA的反应仅在临床疾病HIV血清阳性的受试者中降低。相反，在包括无症状组在内的大多数HIV血清阳性受试者中，对脉宽调制的反应显著降低。对16名HIV血清阳性受试者的进一步分析表明，CD4和CD8T细胞亚群的增殖反应都降低了。共有15名对脉宽调制反应低的HIV血清阳性者，其中7人患有艾滋病，8人为对照组，用于以下研究。研究了T_3、T_1、DeltaR和CD2的表达，发现在HIV血清阳性的非AIDS患者中，CD2受体阳性细胞的百分比增加。研究了正常人PBL对PHA、PWM、CD3抗体或CD2抗体刺激的增殖反应，结果显示，对照组PBL对PHA、CD2ab的刺激反应显著相关，而艾滋病患者仅对PHA和CD2ab的刺激反应相关。对照组对CD2ab和CD3ab的增殖反应大于对PHA和PWM的反应。在患者中，这些反应比对PWM的反应抑制得少，这表明有丝分裂原刺激比简单地刺激Ti/T3和CD2受体要复杂得多。进一步研究静息T细胞，即去除巨噬细胞和预活化细胞的淋巴细胞。加入PHA可诱导细胞预活化，并表达IL-2R(CD25)，但不能促进细胞增殖。相反，加入与CD2受体结合的PHA和SRBC可引起IL-2R的表达、IL-2的产生和增殖。添加PWM+SRBC不会导致细胞增殖。对26例HIV血清阳性者(其中7例为AIDS患者和12例血清阴性者)的静息T细胞对PHA+SRBC的反应进行了比较。结果表明，19例非AIDS患者静息T细胞对PHA+SRBC的反应正常或仅轻微下降，而AIDS患者的静息T细胞反应减弱。然而，所有艾滋病患者在这项检测中都表现出明确的反应。因此，对PHA和PWM的反应之间的差异可以用PHA/CD2依赖的通路的至少部分保留的功能来解释。我们认为，HIV感染引起的缺陷主要与T3/Ti诱导的反应有关。
We studied the proliferative response of PBL to the mitogens PHA and PWM and Candida albicans Ag in 301 HIV seropositive homosexual men, of whom 55 had AIDS. The responses to PHA were reduced only in the clinically ill HIV seropositive subjects. In contrast, the responses to PWM were profoundly reduced in most HIV seropositive subjects including the asymptomatic group. Further analysis of 16 HIV seropositive subjects showed that the proliferative responses were reduced in both CD4 and CD8 T cell subsets. A total of 15 HIV seropositive individuals with low responses to PWM, of whom seven had AIDS and eight controls were chosen for the following studies. Expression of T3, Ti, delta receptors, and CD2 was investigated and showed an increased percentage of CD2 receptors positive cells in HIV seropositive subjects without AIDS. The proliferative responses of PBL to stimulation with PHA, PWM, antibodies to CD3, or antibodies to CD2 were investigated and showed significant correlation in controls, whereas in contrast, only the responses to PHA and CD2ab correlated in patients with AIDS. The proliferative responses to CD2ab and CD3ab in controls were larger than the responses to both PHA and PWM. In patients, these responses were less suppressed than the responses to PWM indicating that stimulation with mitogens is more complex than a simple stimulation of Ti/T3 and CD2 receptors. Further investigations were done on resting T cells, i.e., lymphocytes depleted of macrophages and pre-activated cells. Addition of PHA to these cells resulted in preactivation with expression of IL-2R (CD25) but not in proliferation. In contrast, addition of PHA plus SRBC, which bind to the CD2 receptors caused IL-2R expression, IL-2 production, and proliferation. Addition of PWM + SRBC did not result in proliferation. A comparison of the responses to PHA + SRBC of resting T cells from 26 HIV seropositive individuals, of whom seven had AIDS and 12 seronegative controls, showed that these responses were normal or only slightly decreased in the 19 seropositive men without AIDS whereas it was decreased in AIDS patients. Nevertheless, all AIDS patients showed clear-cut responses in this assay. Thus, the discrepancy between responses to PHA and PWM may be explained by an at least partially preserved function of the PHA/CD2-dependent pathway. We suggest that the defect induced by the HIV infection primarily concerns T3/Ti-induced responses.